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SHOCK Shen Hong Zhejiang University School of Medicine. Historical Aspects The concept of shock has evolved over the centuries from the earliest description in antiquity of traumatic wounds and hemorrhage. Hippocratic facies (460~380 B.C.): tourniguet. Bloodletting Galen (A.D. 130~200): erroneous knowledge of anatomy. Ligation of bleeding vessels Vesalius. William Harvey (16 centuries): anatomy and circulation of the cardiovascular system A French military surgeon: the use of simple bandages Thomas Latta: in 1831. infusion of intravenous fluids into hypovolemic patients inflicted with cholera caused clinical improvent. Pathogenesis: a. vasomotor exhaustion: neurogenic theory b. traumatic toxemia: cannon. Bay(World War I) c. hypovolemia: Keith, Blalock(experiments on dogs) d. fat embolism; e. acidosis f. adrenal dysfunction Pathogenesis: resuscitation, individual argan dysfunction, cellular derangements(Korean, Vietnam conflict). Shock lung. ARDS molecular biology, inflammatory mediator, metabolic support, oxygen delivery, organ ischemia, sepsis. II. Definition of shock A syndrome results from inadequate perfusion of tissues alterations in cellular metabolism, cellular dysfunction and cellular injury, MODS due to tissue hyperfusion, hypoxia. Oxygen delivery; oxygen debt; oxygen demand exceeds the oxygen supply. III. Cause, classification of shock 1. hypovolemic shock 1) hemorrhagic losses: trauma, gastrointestinal bleeding ruptured aneurysm. 2) plasma volume losses: extravascular fluid sequestration, pancreatitis, burns, bowel obstruction. 2. cardiogenic shock dinminished cardiac output intrinsic cause extrinsic cause myocardial infarction cardiac rhythm disturbances. Tension pneumothorax pericardial tamponade 3. neurogenic shock failure of the sympathetic nervous system to maintain normal vascular tone. Spinal cord injury, severe head injury. Spinal anesthesia 4. vasogenic endogenous or exogenous vaso-active mediators systemic inflammatory response syndrome(SIRS) sepsis (infectious) noninfectious Anaphylactic Hypoadrenal traumatic IV. Pathophysiology of shock Impaired tissue perfusion Tissue hypoxia Anaerobic metabolism Inflammatory Mediators Circulatory redistribution Ischemia/ Reperfusion Acidosis Cellular dysfunction SIRS / Sepsis Multiple organ dysfunction syndrome Pathophysiology: Role of hypoxia Anaerobic metabolism and acidosis Hyperlactatemia Circulatory redistribution Impairment of gut perfusion Anaerobic metabolism and acidosis Glycogen Anaerobic glycolysis Aerobic glycolysis Glucose Pyruvate lactate cytosol mitochondria Acetyl CoA Citric Acid cycle Circulatory redistribution Vaso-constrictive factors: Catechol, angiotensin II, vasopressin, endothelin, thromboxan A2 Vaso-dilatory: Nitric oxide, prostaglandin E2, prostacyclin, interleukin-2, bradykinin. Impairment of gut perfusion: Subsequent bacterial or toxin translocation Systemic inflammatory response, MODS I. baroreceptors Vasomotor center(medulla) Sympathetic neural output Increased systemic vascular resistance Increased venous return to the heart Arteriolar vasoconstriction(cutaneous tissue. Skeletal muscle. Renal and splanchnic vascular beds) II. adrenal medullary output↑ tachycardia, enhanced cardiac contractility III. Antidiuretic hormone(posterior pituitary) Vasoconstriction Water reabsorption in the distal tubule of the kidney IV. rennin(kidney) Angiotensin I (liver) Angiotensin II (lungs) vasoconstrictor aldosterone(adrenal of sodium cortex) →reabsorption V. microcirculatory autoregulation Mediator of shock and sepsis Endotoxin Complement fragments Eicosanoids Cytokines: Leukotrienes, Prostaglandins, Throbomxanes Interleukins(IL1, IL2, IL6); TNF-a; CSF, GCSF,GM-CSF; IFN-r Neuroendocrine mediators: catechols, cortisol, glucagons V. diagosis and management of shock: General approach Keep SaO2> 90% Optimize cardiac index supply supplemental O2 mechanical ventilation, if necessary May need early hemodynamic monitoring Optimize Hb 11-13g/dl Assess volume status(preload) PCWP<15 volume expansion PCWP>15 consider volume if PCWP<18 diureses if PCWP>18 Reassess to keep: PCWP 15-18 mmHg MAP 60-80 mmHg SvO2 >65-70% Delivery independent O2 consumption Goals not met Goals met Inotropic support (b agonism) Treat inciting cause of shock Dobutamine control inflammatory response Dopamine nutritional support Epinephrine Reassess Goals met Treat inciting cause of shock control inflammatory response nutritional support Goals not met Consider vasodilators Nitroglycenin Nitroprusside Consider a agonist Norepinephrine Epinephrine Neosynephrine Plus Dopamine SPECIFIC SHOCK SYNDROMES al signs and symptoms of hemorrhagic shock based on severity loss Percent loss of circulating blood volume(volume loss for 70kg male) Pulse rate Systolic pressure Pulse pressure Capillary refi ll Respirations Central nervo us syste m Urine output <15%(<750ml) 15%-30%(7501500ml) 30%-40%(15002000ml) >40%(>2000ml) normal >100 >120 >140 nonpalpab le normal normal weak decreased marked decreased normal decreased decreased marked decreased normal delaye d delaye d absent Normal Mild tachypnea Marked tachypnea Marked tachypnea normal anxious confused lathargic normal 2030ml /hr 20ml/hr negligible Traumatic shock Hypovolemic shock with 1. larger volume losses 2. greater fluid sequestration in the extravascular compartments 3. more intense activation of inflammatory mediators development of SIRS 4. microcirculatory derangements 5. MODS frequently occur Traumatic shock treatment 1. excessive fluid requirements 2. mechanical ventilation 3. pulmonary artery catheter monitoring 4. cardiovascular support Shock Associated with SIRS, Sepsis, and MODS SIRS: two or more of following 1. temperature greater than 38℃ or less than 36℃ 2. heart rate greater than 90 beats per minute 3. respiratory rate greater than 20 breaths per minute or PaCO2 less than 32mmHg 4. white blood cell count greater than 12,000 per cu mm, less than 4000 per cu mm or greater than 10% band forms VII. Diagnosis of hypovolemic shock 1. clinical history; 2. physical findings; 3. blood tests. 4. characteristic hemodynamics 1. low right and left sided filling pressures(low central venous pressure, low PCWP) 2. decreased cardiac output, decreased SvO2 3. increased systemic vascular resistance VIII. Treatment Patients airway; adequate ventilation, oxygenation Fluid replacement isotonic electrolyte solutions Crystalloid --- Ringer’s lactate solution Blood transfusion --- type-specific type O packed red blood cells Guide treatment If absent monitor the central venous pressure Place a pulmonary artery catheter Then: urinary output rate of 0.5 to 1.0 ml/kg/hour The pneumatic anti-shock garment Colloid solution; hyper-tonic saline(controversy) SEPSIS Sepsis: the presence of SIRS in association with culture-proven infection Septic shock: sepsis with hypotension despite adequate fluid resuscitation, along with the presence of manifestations of hypoperfusion, including, but not limited to, lactic acidosis, oliguria, or an acute alteration in mental status. Mutiple organ dysfunction syndrome (MODS): the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention. Mortality rate 26% SIRS→Sepsis Mortality rate: 7%→16% 4%Sepsis→Septic shock Mortality rate: 7%→46% MODS mortality range from 20% to 100% depending on the number of failed organs severity of illness scoring systems MODS Primary MODS Ischemic Reperfussion direct insult Secondary MODS(two-hit model) exaggerated uncontrolled systemic inflammatory response clinical features: fever, tachycardia, hypotension, oliguria (obtundation, coma)altered mental status. Leukocytosis or leukopenia increased or decreased systemic vascular resistance. Positive microbial cultures gram-negative bacteria escherichia coli, klebsiella pseudomonas staphylococcus streptococcus spices,fungal, viral , protozoal pneumonia, gastrointestinal perforation biliary tract infection, urinary tract infection burn wounds The Two-hit Theory of MODS First Hit Systemic Inflammatory response 1° MODS Death Amplified Systemic Inflammation response Second Hit Recovery 2° MODS Recovery Death 1. Pulmonary failure ARDS Mortality exceeds 50% ventilation perfusion abnormalities pulmonary edema hypoxemia decreased functional residual capacity decreased infiltrates on chest X-rays 2. Gastrointestinal dysfunction Gastritis. Ulcerations. Pancreatitis; cholesystitis, mal-absorption, mucosal atrophy, translocation of bacteria or toxins. 3. Renal dysfunction Tissue hypoperfusion Tissue damage by activated infalammatory cells and their mediators Uremia electrolyte disturbances dialysis 4. Cardiac dysfunction 1 depreesed coronary blood flow 2 direct endotoxin toxicity 3 myocardia depressant factor(TNF) 5. CNS manifestation of MODS GCS scoring; mental status the patients’ best eye opening, verbal and motor responses Treatment To prevent the progression to MODS. To improve oxygen delivery and oxygen comsumption Oxygen delivery: Volume expansion;Provision of red blood cell mass;Use of pharmacologic agents:Beta agonists & Vasodilators For monitoring: e.g. pulmonary artery catheter For hemodynamic and other physiologic evaluation Antibiotics: to detect possible sources of infection(culture) Surgical debridement Drainage Nutritional support The End